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HRAS 1 and INS genes are relocated but not structurally altered as a result of the t(7;11) (p15;p15) in a clone from a patient with acute myeloid leukaemia (M4)
Author(s) -
Morris C. M.,
Fitzgerald P. H.,
Kennedy M. A.,
Hollings P. E.,
Garry M.,
Corbett G. M.
Publication year - 1989
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1989.tb06306.x
Subject(s) - breakpoint cluster region , biology , chromosomal translocation , abl , gene , chromosome , microbiology and biotechnology , breakpoint , clone (java method) , chromosome 7 (human) , acute myelomonocytic leukemia , chromosome 9 , hras , genetics , leukemia , mutation , signal transduction , tyrosine kinase , kras
S ummary . A patient whose leukaemic cells carried the rare t(7;11)(p15;p15) was diagnosed as having acute myelomonocytic leukaemia (AML‐M4), and supports the association of this specific translocation with forms of acute myeloid leukaemia showing differentiation. Blast phase chronic myeloid leukaemia was excluded by lack of involvement of the ABL and BCR genes. Chromosome in situ hybridization studies showed that both the HRAS 1 and INS genes were present on the terminal part of chromosome 11p which was translocated to chromosome 7p. Neither HRAS 1 nor INS were structurally rearranged. Field inversion gel electrophoresis showed that a 400 kb fragment encompassing HRAS 1 was structurally entire in leukaemic DNA. Because the INS gene, which was also translocated, is probably located proximal to HRAS 1 on chromosome 11p. it is unlikely that HRAS 1 was near the chromosome 11 breakpoint or involved in this leukaemia.